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September 1939

EXPERIMENTAL STUDY OF PATHOGENESIS OF CEREBRAL CHANGES FOLLOWING PROLONGED INSULIN HYPOGLYCEMIA

Author Affiliations

With the Technical Assistance of John F. Iannucci NEW HAVEN, CONN.

From the Department of Pediatrics, Yale University School of Medicine.

Arch NeurPsych. 1939;42(3):395-402. doi:10.1001/archneurpsyc.1939.02270210033002
Abstract

In a previous communication1 we presented the results of the chemical analyses of the brains of cats which survived severe insulin shock without treatment. Clinically, these animals presented a picture best described as that characteristic of decerebrate rigidity. The symptoms included lack of response to the environment, insensibility to painful stimuli, gross impairment of gait and increased extensor tonus of the extremities. Chemically, evidences of a marked disturbance in the distribution of water and electrolytes in the brain were demonstrated. These were interpreted as secondary to widespread cellular injury and were considered manifestations of cellular disintegration of varying degrees. This was confirmed by histopathologic examination of the involved brains,2 which revealed widespread necrobiosis of the ganglion cells of the cortex, basal ganglia and upper part of the medulla. Histologic evidence of comparable nature demonstrating damage to the central nervous system as a result of insulin hypoglycemia in animals,

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